Incarceration, polygenic risk, and depressive symptoms among males in late adulthood

2021 ◽  
pp. 102683
Author(s):  
Hexuan Liu ◽  
Peter T. Tanksley ◽  
Ryan T. Motz ◽  
Rachel M. Kail ◽  
J.C. Barnes
Author(s):  
Nils Kappelmann ◽  
Darina Czamara ◽  
Nicolas Rost ◽  
Sylvain Moser ◽  
Vanessa Schmoll ◽  
...  

PLoS ONE ◽  
2017 ◽  
Vol 12 (12) ◽  
pp. e0189683 ◽  
Author(s):  
Paul Kenneth Hitchcott ◽  
Maria Chiara Fastame ◽  
Dalila Langiu ◽  
Maria Pietronilla Penna

Author(s):  
Stefanie A. Nelemans ◽  
Marco Boks ◽  
Bochao Lin ◽  
Tineke Oldehinkel ◽  
Pol van Lier ◽  
...  

AbstractResearch has focused more and more on the interplay between genetics and environment in predicting different forms of psychopathology, including depressive symptoms. While the polygenic nature of depressive symptoms is increasingly recognized, only few studies have applied a polygenic approach in gene-by-environment interaction (G × E) studies. Furthermore, longitudinal G × E studies on developmental psychopathological properties of depression are scarce. Therefore, this 6-year longitudinal community study examined the interaction between genetic risk for major depression and a multi-informant longitudinal index of critical parenting in relation to depressive symptom development from early to late adolescence. The sample consisted of 327 Dutch adolescents of European descent (56% boys; Mage T1 = 13.00, SDage T1 = 0.44). Polygenic risk for major depression was based on the Hyde et al. (Nature Genetics, 48, 1031–1036, 2016) meta-analysis and genetic sensitivity analyses were based on the 23andMe discovery dataset. Latent Growth Models suggested that polygenic risk score for major depression was associated with higher depressive symptoms across adolescence (significant main effect), particularly for those experiencing elevated levels of critical parenting (significant G × E). These findings highlight how polygenic risk for major depression in combination with a general environmental factor impacts depressive symptom development from early to late adolescence.


2018 ◽  
Vol 213 (4) ◽  
pp. 579-586 ◽  
Author(s):  
Changwei Li ◽  
Toni Miles ◽  
Luqi Shen ◽  
Ye Shen ◽  
Tingting Liu ◽  
...  

BackgroundThe Chinese Great Famine caused widespread starvation in 1959–1961. Its long-term association with depressive symptoms has not been studied.AimsTo estimate the burden of depressive symptoms and the association of famine exposure with depressive symptoms.MethodThe China Health and Retirement Longitudinal Study is a nationwide representative survey of 17 708 Chinese adults aged ≥45. Propensity score matching and modified Poisson regression were used to evaluate the association between self-reported famine exposure in early life and depressive symptoms among the overall participants. Such associations were also assessed by developmental stage using modified Poisson regression and logistic regression.ResultsThe prevalence of depressive symptoms was 26.2% (95% CI 25.1–27.3%) in 2011. As defined by loss of family members because of starvation, 11.6% (95% CI 10.1–13.1%) of this population experienced severe famine. When compared with participants who did not experience starvation, those who had experienced severe famine during fetal, mid-childhood, young-teenage and early-adulthood stages had 1.87 (95% CI 1.36–2.55), 1.54 (95% CI 1.23–1.94), 1.47 (95% CI 1.09–2.00) and 1.77 (95% CI 1.42–2.21) times higher odds of having depressive symptoms in late adulthood, respectively. The first two trimesters of pregnancy were a critical time window during the fetal stage when severe famine had a stronger association with depressive symptoms. Famine during infant, toddler, preschool or teenage stages was not associated with depressive symptoms. Overall, famine contributed to 13.6% of the depressive symptom burden in this population.ConclusionsThe Chinese Great Famine contributed substantially to the burden of depressive symptoms in China.Declaration of interestNone.


2020 ◽  
Vol 30 (12) ◽  
pp. 6121-6134 ◽  
Author(s):  
H Acosta ◽  
K Kantojärvi ◽  
N Hashempour ◽  
J Pelto ◽  
N M Scheinin ◽  
...  

Abstract Psychiatric disease susceptibility partly originates prenatally and is shaped by an interplay of genetic and environmental risk factors. A recent study has provided preliminary evidence that an offspring polygenic risk score for major depressive disorder (PRS-MDD), based on European ancestry, interacts with prenatal maternal depressive symptoms (GxE) on neonatal right amygdalar (US and Asian cohort) and hippocampal volumes (Asian cohort). However, to date, this GxE interplay has only been addressed by one study and is yet unknown for a European ancestry sample. We investigated in 105 Finnish mother–infant dyads (44 female, 11–54 days old) how offspring PRS-MDD interacts with prenatal maternal depressive symptoms (Edinburgh Postnatal Depression Scale, gestational weeks 14, 24, 34) on infant amygdalar and hippocampal volumes. We found a GxE effect on right amygdalar volumes, significant in the main analysis, but nonsignificant after multiple comparison correction and some of the control analyses, whose direction paralleled the US cohort findings. Additional exploratory analyses suggested a sex-specific GxE effect on right hippocampal volumes. Our study is the first to provide support, though statistically weak, for an interplay of offspring PRS-MDD and prenatal maternal depressive symptoms on infant limbic brain volumes in a cohort matched to the PRS-MDD discovery sample.


2014 ◽  
Vol 45 (8) ◽  
pp. 1709-1720 ◽  
Author(s):  
K. L. Musliner ◽  
F. Seifuddin ◽  
J. A. Judy ◽  
M. Pirooznia ◽  
F. S. Goes ◽  
...  

Background.Previous studies suggest that the relationship between genetic risk and depression may be moderated by stressful life events (SLEs). The goal of this study was to assess whether SLEs moderate the association between polygenic risk of major depressive disorder (MDD) and depressive symptoms in older adults.Method.We used logistic and negative binomial regressions to assess the associations between polygenic risk, SLEs and depressive symptoms in a sample of 8761 participants from the Health and Retirement Study. Polygenic scores were derived from the Psychiatric Genomics Consortium genome-wide association study of MDD. SLEs were operationalized as a dichotomous variable indicating whether participants had experienced at least one stressful event during the previous 2 years. Depressive symptoms were measured using an eight-item Center for Epidemiologic Studies Depression Scale subscale and operationalized as both a dichotomous and a count variable.Results.The odds of reporting four or more depressive symptoms were over twice as high among individuals who experienced at least one SLE (odds ratio 2.19, 95% confidence interval 1.86–2.58). Polygenic scores were significantly associated with depressive symptoms (β= 0.21,p⩽ 0.0001), although the variance explained was modest (pseudor2= 0.0095). None of the interaction terms for polygenic scores and SLEs was statistically significant.Conclusions.Polygenic risk and SLEs are robust, independent predictors of depressive symptoms in older adults. Consistent with an additive model, we found no evidence that SLEs moderated the association between common variant polygenic risk and depressive symptoms.


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